Cardiac Patient Flashcards
Treatment of the CV patient requires multiple avenues of treatment:
- diet
- medication
- exercise
- stress reduction
- smoking cessation
- integrate your treatment
Cardiac Sympathetics
- origins in T1-6 with synapses in the upper thoracic and cervical chain ganglia
- fibers originating from the right pass to the right deep cardiac plexus
- fibers originating from the left pass through the left deep plexus and inverted AV node
Right deep cardiac plexus
- innervates the SA node
- hyperactivity predisposes to supraventricular tachyarrhythmias
Left deep cardiac plexus
- innervates AV node
- hyperstimulation predisposes to ectopic foci and ventricullar fibrillation
Increased sympathetic tone linked to
- coronary vasospasm
- associated with increased morbidity post-MI (inhibits collateral circulation development)
Vessels are rich in sympathetics:
- vasoconstriction: increases peripheral vascular resistance; produces a shunt from one area to another
- decreased tone=vasodilation
Cardiac Parasympathetics
- right vagus nerve primarily to SA node
- left vagus nerve supplies AV node
- visceral-visceral reflexes
Right vagus nerve hyperactivity
-leads to sinus bradyarrythmias
Left vagus nerve hyperactivity
leads to AV block
Visceral-visceral reflexes
-pulmonary branches strongest inhibitor reflex–aspiration
Visceral-visceral reflexes (slowing of heart rate)
- irritation of larynx
- pressure on carotid body
- pressure on globe of eye (oculocardiac reflex): less affect in sympathecotonic patients; more affective in vagotonia patients
Vagal connections abundant at
OA, AA and C2 areas
PNS Vasculature involvement
- submaxillary gland vessels
- parotid gland vessels
- vessels of blush region of face
- vessels of tongue
- vessels of the penis
Cardio Lymphatics
- drainage from the heart and lungs mainly via the right lymphatic duct
- impaired drainage known to severely compromise homeostatic mechanisms: increased morbidity and mortality with ischemia and infection
- peripherally, lymphatic congestion has been linked to atherosclerosis and HTN
Lymphatics play significant role in
- pulmonary edema
- ascites
- hepatomegaly
- peripheral edema in CHF: electrolyte imbalance develops; increases morbidity
Thoracic duct
- under sympathetic control
- hypersympathetic activity can reduce flow
Somatic involvement in Cardiac disease
- severe scoliosis (75 degrees thoracic curve) compromises cardiac function
- compensatory musculoskeletal problems reflexly affect cardiac function
- must treat postural stressor
- longer lasting changes to compensatory changes with OMM
Somatic involvement in cardiac disease: gait
- in patients with decreased cardiac output, abnormal gait patterns increase cardiac workload up to 300%
- optimizing the gait pattern will give back strength to fulfill activities of daily living
Somatic involvement in cardiac disease: anterior chest wall syndrome
- generic term for a variety of causes for substernal and/or chest pains
- often misdiagnosed as cardiac dysfunction
- somatic factors do co-exist with cardiac disease
- reduction in cardiac symptoms after OMM cannot rule out the need for further work-up or therapeutics in a given patient
Somatic causes of chest pain
- cervical, thoracic, sternal, rib dysfunction
- costochondritis (Tietze’s syndrome)
- intercostal neuritis
- myofascial trigger points–pec major and minor
- rib fractures
Classic cardiac and coronary pattern of pain referral
- upper left chest radiating out and down the inner surface of the arm and up into the neck and jaw
- palpatory changes found mostly at levels of T2-4 on the left
Anterior wall infarctions have more changes in
T1-4
Pain referral: posterior and inferior wall MI
- increased bradyarrhythmias
- palpatory changes at C2: rich in vagal connections
- may have an autonomic rationale for these changes
Hypertension is strongly associated with
bilateral trophic changes at T5-7, T8-T10, and T11-L2
- study controlled for age, sex, and other comorbid condition
- diabetes T10-11
Myocardial infarction
- first treatment goal is to decrease SNS activity in upper thoracics
- reduce inappropriate reflexes
- lower risk of ectopic foci and ventricular fibrillation
- remove at least one factor that discourages collateral circulation
- use indirect techniques: paraspinal inhibition (lower peripheral resistance)
MI Vagal stimulation
- C2 and cranial base
- inferior wall infarction
- treat these areas to help decrease bradyarrhythmias, hypotension, and decreased coronary flow to ischemic tissue
MI: Sympathetics
- SNS stimulation of T1-6
- more activity at T2-3 on the left: anterior wall infarction
- treat these areas to help decrease risk of supra ventricular and ventricular arrythmias
Myocardial Infarction: Lymphatics
- treat thoracic inlet indirectly
- if post-resuscitation: indirect treatment to ribs and sternum
- pectoral traction; diaphragm addressed through thoracolumbar fascia (indirect)
Hypertension: Multifactorial etiology
- genetic
- habitual factors
- neurogenic
- humoral (hormonal)
- vascular
HTN functional elements implicated
- vascular and cardiac hyper-reactivity to sympathetic stimuli in most patients with HTN
- prolonged SNS stimulation to kidneys leads to water and sodium retention
- As BP increases, homeostatic mechanisms of the baroreceptors reset to maintain higher arterial pressure
HTN Treatment
- aimed at supporting the homeostatic mechanisms
- Address the kidney and adrenal areas–actively involved in body homeostasis
- Treat the whole spine: sympathetic innervation involves the entire spinal column
- involves respiratory/fluid, neurologic and energy model
HTN Chapman’s points
- posterior T11-12
- treatment by rotatory stimulation
- systolic BP drop 15 mmHg
- diastolic BP drop 8 mmHg
- aldosterone down in 36 hours
Congestive Heart Failure
- diagnosis not just a symptom
- find the cause and address it
- treatment emphasis on: lymphatics and autonomics
- when lymphatic channels are full and obstructed fluids “third space”–peripheral edema
- thoracic duct dilation may occur with leakage causing ascites
CHF Treatment
- increased venous and lymphatic return will help increase cardiac output (especially after MI)
- treat the thoracolumbar diaphragm: optimize the lymphatic pump
- treatment to thoracic cage also helps with pumping mechanism
- lymphatic pump and eflleurage/petrassage
Arrythmia Treatment
- modify vagal tone–oculocardiac reflex; carotid sinus; valsalva; OA/AA/C2
- reduce segmental facilitation in the upper thoracics–addresses sympathetics
